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Pathophysiology > Cancer (Exam 2) > Flashcards

Cancer (Exam 2) Flashcards

1
Q

controlled cell division and growth impact what

A

organ development during embryogenesis, tissue homeostasis, tissue repair, and remodeling

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2
Q

normal cells are restricted in

A

their capacity to divide and grow and will not survive indefinitely

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3
Q

cell cycle

A

series of events by which normal and cancer cells divide to produce new cells

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4
Q

what is the cell cycle very strict in?

A

very strictly regulated in healthy cells

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5
Q

5 phases of cell cycle

A

DNA replication (S phase)
cell division (M phase)
2 resting phases (G1 and G2)
non-dividing state (G0 phase)

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6
Q

m phase

A

cell division - cell divides

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7
Q

G1 phase

A

resting phase - cell grows in size and decides to commit to the cell cycle or remain in a resting state

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8
Q

S phase

A

DNA replication - cell synthesizes (duplicates) its DNA

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9
Q

G2 phase

A

resting phase - cell prepares to divide

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10
Q

G0 phase

A

non-dividing state - the cell stops dividing and may differentiate

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11
Q

what determines if the cycle should proceed?

A

integrated signal input from oncogenes and tumor suppressors

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12
Q

what is the cell cycle mainly composed of and its promotion?

A

cyclins and cdk’s (cyclin-dependent kinases) and promotes progression through each phase

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13
Q

when in normal state, what starts the cycle?

A

receiving an external signal to divide
ex: growth factor binding at cell surface

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14
Q

G1 phase progression

A

cdk4/cyclin D, cdk6/cyclin D

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15
Q

S phase progression

A

cdk2/cyclin E, cdk2/cyclin A

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16
Q

G2 phase oncogenes

A

cdk1/cyclin A

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17
Q

M phase oncogen

A

cdk1/cyclin B

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18
Q

cell cycle checkpoints

A

elaborate system of molecular events is in place in each phase to prevent progression if the cell is damaged or the environment is unfavorable for growth

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19
Q

M phase checkpoint

A

check for proper attachment of chromosomes to spindles

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20
Q

G1 phase checkpoint

A

check for environmental cues, growth factor signals, nutrient availability, DNA damage, restriction site: retinoblastoma protein

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21
Q

G2 phase checkpoint

A

check for cell size, damaged DNA, unreplicated DNA

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22
Q

S phase checkpoint

A

check for DNA damage, ensure all DNA is replicated

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23
Q

cell cycle regulation

A

controls regulated the rate of cell proliferation and growth and can cause cancer if they are mutated

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24
Q

oncogene

A

normally promotes cell cycle progression, can induce uncontrolled cell division if mutated,
-cdk’s and cyclins
-E2F

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25
Q

tumor suppressor

A

normally prevents cell cycle progression, can induce uncontrolled cell division if mutates

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26
Q

p16, p21, p27, p57

A

suppress CDK activity

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27
Q

p53

A

senses DNA damage and activates P21

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28
Q

pRb

A

suppresses E2F activity

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29
Q

what do growth factors activate?

A

the cell cycle when they bind to cell surface receptors

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30
Q

growth factors

A

stimulate proliferation of many different type of cells growth factors can have different effects in different cell types.

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31
Q

what do growth factors bind to?

A

specific receptors in the plasma membrane and activate signaling pathways and consist of kinases cascades

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32
Q

what happens when kinases cascades are phosphorylated?

A

they will phosphorylate (activate) another kinase

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33
Q

growth factor pathways

A

lead to activation of nuclear kinases and changes in gene transcription that cause cell survival and cell cycle progression

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34
Q

growth factor pathway components

A

Phospholipase C (PLC)/ Protein C (PKC)
PI3K/Akt
RAS/RAF/MEK/ERK

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35
Q

growth factor pathways from individual growth factors do what?

A

overlap and amplify a response to proliferate

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36
Q

mutated growth factor receptors and signaling proteins can trigger what?

A

uncontrolled cell division

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37
Q

inhibitory signaling pathways from other growth factors can..?

A

suppress a response to proliferate

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38
Q

what do normal cell division and growth rely on?

A

expression of proteins encoded in DNA

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39
Q

what is DNA expression regulated by?

A

epigenetics

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40
Q

what does wrapping DNA around histone proteins allow?

A

allows DNA to be compacted into chromosomes and can determine whether a gene will be expressed or not

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41
Q

enzymes that compact chromatin

A

DNMT: DNA methyltransferase
HDAC: histone deacetylase

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42
Q

enzymes that loosen chromatin

A

HAT: histone acetyltransferase

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43
Q

histone modifications

A

regulated by environmental factors (toxin exposure, smoking, alcohol, exercise, diet)
behaviors affect heritable patterns of gene expression via epigenetics

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44
Q

heterochromatin

A

tightly packed nucleosomes
gene is silenced

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45
Q

euchromatin

A

loosely packed nucleosomes
gene is expressed

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46
Q

why is a gene silenced?

A

methylation of DNA and histones causes nucleosomes to pack tightly together. transcription factors cannot bind the DNA, and genes are not expressed

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47
Q

why are genes expressed?

A

histone acetylation results in loose packing of nucleosomes. transcription factors can bind the DNA and genes are expressed

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48
Q

apoptosis

A

programmed cell death
normal process required for tissue homeostasis, also will kill cells that are abnormal
regulated by tumor suppressors and oncogenes

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49
Q

what can prevent apoptosis?

A

over-expression of oncogenes (Bcl-2)

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50
Q

cellular senescence

A

a cell stops growing and dies after a certain number of divisions

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51
Q

what are cellular senescences regulated by?

A

telomeres

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52
Q

telomeres

A

DNA sequence of caps at ends of chromosomes that protect ends of DNA from damage
shorten after each replication, once at a critical length cells senesce

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53
Q

telomerase

A

enzyme that adds DNA to telomeres - over expression can inhibit telomere shortening and prevent normal cell senescence

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54
Q

DNA repair

A

mechanisms composed of several enzymes that identify and repair damage to DNA

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55
Q

how can DNA be mutated?

A

by exposure to environmental factors (UV irradiation, cigarette smoke, X-rays) or by effects of normal cellular processes such as DNA replication

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56
Q

how many cells does the human body contain?

A

about 37 trillion cells, each cell having about 3 billion bases

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57
Q

mutation rate per cell

A

quite low
10-8 - 10-7 mutations per nucleotide per cell division

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58
Q

what does each cell in the body experience every day?

A

about 10,000 DNA lesions due to normal metabolic processes and environmental exposures; most of these lesions are repaired

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59
Q

DNA repair mechanism

A

detection of mutation

removal of mutated DNA (usually with some surrounding normal DNA)

re-synthesis of correct DNA using other strand in double helix: polymerases

sealing the ends of the newly synthesized DNA to the surrounding DNA: ligases

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60
Q

immune surveillance

A

human t cells can recognize cancerous cells as foreign

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61
Q

antigen presenting cells (APCs)

A

pick up antigens released from tumor cells APCs activate T cells to recognize tumor antigens. T cells find tumor cells and kill them

62
Q

neoplasia

A

new or abnormal cell growth characterized by loss of tissue homeostasis and distorted architecture

63
Q

benign tumor

A

abnormal cell growth confined to one specific tissue site; few systemic manifestations and no threat to overall state of healthc

64
Q

cancer or malignant tumor

A

a more advanced form of neoplasia that involves tissue and damage; a progressive process that can culminate in systemic disease and death

65
Q

tumor/neoplasm

A

growth resulting from disordered regulation of a cell cycle

66
Q

what do most cancers show?

A

unlimited cell division and impaired differentiation

67
Q

cancer biomarker

A

a gene or protein that is altered in expression in cancer and can be used to identify a type of cancer

68
Q

cancer progression

A

characterized by an accumulation of genetic alterations that cause morphological changes in cells within a tissue

69
Q

hypertrophy

A

enlargement of cells (too much protein and membrane)

70
Q

hyperplasia

A

higher than normal cell division, causing crowding of cells

71
Q

dysplasia

A

cells revert to an immature, less differentiated state, causing disordered growth

72
Q

metaplasia

A

cells appear and function like cells of a different type

73
Q

genotoxic agents

A

induce DNA mutations

74
Q

non-genotoxic agents

A

do not induce DNA mutations, on their own, usually accelerate cell division in other ways

75
Q

chemical carcinogens metabolic reactions

A

convert many carcinogens to highly reactive molecules that can react with nucleotides in DNA

DNA adduct disrupts structure of DNA helix

76
Q

chemical carcinogens altered structure of DNA

A

adduct causes nucleotide to mispair during replication, resulting in a mutation that can be propagated to progency cells

77
Q

ionizing radiation

A

very severe
can lead to chromosomal abnormalities
can also induce mutations and cell death

78
Q

non-ionizing radiation

A

less severe
may stall replication and transcription
can also induce mutations

79
Q

microbial carcinogens

A

pathogenic bacteria can induce carcinogenesis in several ways (direct and indirect)

80
Q

altering intracellular signaling pathways

A

stimulate proliferation of human cells
induce chronic inflammation
product toxins and ROS that damage human DNA
trigger a stem cell-like phenotype

81
Q

microbiome

A

composition of microbes in a tissue environment; often a critical factor in promoting or preventing tumorigenesis

82
Q

how can viruses induce carcinogenesis?

A

stimulate uncontrolled proliferation of human cells by
expressing proteins that inactivate tumor suppressors and inhibit apoptosis
inserting in human genome near oncogenes and activating their expression: induce chronic inflammation, mutations by gene integration that interrupts DNA sequence

83
Q

HPV proteins

A

E6 protein targets p53 for destruction
E7 protein sequesters Rb

84
Q

spontaneous mutations

A

changes to DNA sequences that occurs in a cell without any known induction by an environmental mutagen

85
Q

rate of spontaneous mutations in humans

A

1.4 x 10^8 mutations per nucleotide per cell generation
with about 6 million nucleotides in the human genome that means about 84 mutations in each cell per cell division

86
Q

spontaneous mutations sources

A

errors in DNA replication
spontaneous lesions
transposable elements “jumping genes”

87
Q

spontaneous mutations during replication

A

slippage of DNA polymerase at nucleotide repeats can cause strand misalignment and induce deletions or insertions

88
Q

spontaneous mutations caused by DNA lesions

A

depurination: loss of purine base
deamination: change of cytosine to uracil

89
Q

ROS

A

formed under high metabolic stress
can alter guanine so that it can pair with adenine

90
Q

depurination and deamination result

A

result in incorporation of an incorrect nucleotide in the DNA sequence during replication

91
Q

spontaneous mutations caused by transposons

A

DNA sequences encoding enzymes that, when expressed, cause the DNA sequence to be inserted into another location in the genome
can insert within a gene and disrupt its function, causing diseases including cancer

92
Q

frequency of jumping

A

about 1 new insertion occurs in 10-100 live births

93
Q

defects in DNA repair pathways

A

induce many gene mutations
- if mutations inactivate the function of important genes in these pathways, DNA damage will not be required

94
Q

results in DNA repair pathways

A

many mutations (1000s) per cell this increases the chance that a cell will undergo carcinogenesis

95
Q

chromosomal instability

A

condition whereby large segments of the genome may be gained, lost, or rearranged due to defects

96
Q

chromosomal instability defects

A

replication and distribution of a full set of sister chromatids to daughter cells during mitosis

97
Q

aneuploidy

A

having an abnormal number of individual chromosomes

98
Q

structural rearrangements

A

alter gene function and expression

99
Q

what can cancer result from?

A

mutations in DNA

100
Q

point mutation

A

changing a single nucleotide to another
- silent mutation
- missense
- nonsense

101
Q

silent mutation

A

no effect

102
Q

missense

A

change amino acid

103
Q

nonsense

A

premature stop codon

104
Q

insertion or deletion

A

adding or removing 1 or more nucleotides
- frameshift mutation

105
Q

frameshift mutation

A

changes reading frame of ribosome, alters all sequence afterward

106
Q

what can lead to carcinogenesis?

A

if a mutation changes the function of a protein that controls cell proliferation of survival

107
Q

genes that are known to be mutated in cancer

A

proto-oncogene

108
Q

proto-oncogene

A

confers an advantage to tumor cells through a gain of function mutation
- less common because very specific mutations are required to activate function

109
Q

proto-oncogene mutated form

A

oncogene
mutation of 1 out of 2 alleles is necessary to alter protein function

110
Q

proto-oncogene activation

A

through mutation, gene amplification and overexpression, chromosomal translocation

111
Q

tumor suppressor

A

confers an advantage to tumor cells through a loss of function mutation
- more common because can inhibit a proteins function or expression

112
Q

tumor suppressor change in function

A

results from nonsense, missense, frameshift, and deletion/insertion mutations

113
Q

without cell cycle control…

A

cancer cells continue to proliferate
- without growth inducing signals
- with damaged DNA
- without proper duplication and segregation of chromosomes

114
Q

common oncogenes activated

A

ckd4/cdk6: activated in many cancers
cdk1
cyclin D

115
Q

tumor suppressors inactivated

A

p53: 50% of cancers have this mutation
p16

116
Q

what do mutated genes encode?

A

proteins that overactivate growth factor signaling pathways., causing them to be constitutively activated even in the absence of growth factor signal from the cell environment

117
Q

examples of oncogenes in growth factor signaling pathways

A

EGFR
HER2
Ras
Raf

118
Q

example of common tumor suppressor in growth factor signaling pathways

A

PTEN

119
Q

what do cancer cells experience?

A

experiences that would usually trigger apoptosis like unrepaired DNA, metabolic stress, hypoxia

120
Q

what do cancer cells disrupt?

A

apoptotic mechanisms and survive with accumulating damaged even with chemotherapy

121
Q

Bcl-2

A

frequently overexpressed

122
Q

p53

A

frequency mutated or deleted

123
Q

telomere in healthy cells

A

telomeres shorten with every cell division
over time crisis point is reached where chromosome ends cant be replenished and cells eventually die

124
Q

telomere in cancer cells

A

telomeres don’t shorten with every cell division chromosome ends are continually replenished, cells survive and grow uncontrollably.

125
Q

telomerase

A

can lengthen telomeres normally expressed in germ cells and early embryonic cells and early embryonic cells not expressed much at all in somatic cells after birth

126
Q

clinical phase of cancer

A

defined by recognition of overt malignancy by symptoms or physical exams

127
Q

preclinical phase of cancer

A

usually unknown to pt, may be identified by screening interventions
- colon polyps, lumps in breast tissue
- usually harbor molecule genetic abnormalities and exhibit features of abnormal proliferation without demonstrating invasiveness

128
Q

initiation

A

exposure of cells to carcinogens or errors in DNA synthesis that cause DNA mutations

129
Q

selective growth advantage

A

a clonal population of abnormal cells can develop

130
Q

what mutations have no effect?

A

b and c

131
Q

what mutants select for growth advantage over normal cells?

A

a, d, and e

132
Q

original mutation

A

cause increase in proliferation that leads to the possibility of more mutations

133
Q

promotion

A

repeated exposure of carcinogens or other factors favor selective expansion of altered cells compared to normal ones
- they are reversible

134
Q

how do promotions act?

A

through multiple ways to increase proliferation and or decrease apoptosis by changing gene expression

135
Q

conversion or malignant transformation

A

changing a preneoplastic cell into one that expressed a malignant phenotype

136
Q

progression

A

accumulation of further genetic and epigenetic changes that lead to increase proliferation

137
Q

progression interactions

A

between tumor cells and surrounding normal stromal cells as well as between tumor cells and the extraceullular matrix

138
Q

how long does it take cancer to develop?

A

decades

139
Q

CIS carcinoma in situ

A

still has defined boarders, does not metastasize

140
Q

germline mutation

A

a genetic alteration that is inherited and is present in every cell of the body
- transmitted to next generation

141
Q

somatic mutation

A

genetic alteration that is not inherited and is not present in every cell of the body but is aquired during a person’s lifetime
- will not be transmitted to next generation

142
Q

familial cancer syndromes

A

often caused by loss of function of proteins involved with DNA repair, causing an increase the mutation rate of the genome
- can increase risk of cancer

143
Q

angiogenesis

A

growth of new blood vessels
remodel blood vessel network, occurs before adulthood and in wound healing ,menstrucal sycle, muscle growth and regeneration of organ lung

143
Q

tumor angiogenesis

A

tumor induced growth of new blood vessels induced by cancer cells

144
Q

what cells can induce their own blood supply?

A

cancer cells

145
Q

angiogenic cytokines

A

induced by hypoxic environment in tumor

146
Q

vascular endothelial growth factor

A

produced by tumor cells, induces proliferation of endothelial cells. target for many anti tumor therapies.

147
Q

platelet derived growth factor

A

produced bu tumor cells and endothelial cells

148
Q

fibroblast growth factor

A

produced by tumor cells

149
Q

matrix metalloproteinases

A

remodel extraceullular matric, mady but stomach cells

Pathophysiology (16 decks)

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